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The B-cell lymphoma 2 (BCL-2)-related ovarian killer (BOK) shares sequence homology with the proapoptotic BCL-2 family members BAX and BAK. However, Bok  −/−  cells are not protected from classic apoptotic triggers and evidence for a proapoptotic role of BOK is derived mostly from overexpression studies (1). BOK localizes preferentially to the endoplasmic reticulum (ER) membrane, where it interacts with IP3-receptors (2, 3). Using cells from their newly generated Bok  −/−  mouse strain, Carpio et al. propose that BOK is a critical inducer of BAX/BAK-dependent apoptosis in response to ER stress (4). This proposal is in contrast to our earlier report, in which we showed that loss of BOK did not confer resistance toward ER stress in several cell types (2). Underlying reasons for this discrepancy may lie in the initial Sv129:C57BL/6 mixed genetic background of the strain used by Carpio et al. (4) [which may influence the phenotype despite backcrossing (5)] and their targeting strategy of the Bok locus. By targeting exons 2 (containing the START codon) and 3, alternative splicing of exon 1–4 is enabled and is indeed readily detectable based on the RT-PCR analysis in figure 1C of Carpio et al. (4). A resulting ∼1-kb transcript (exon1/4/5), which is not occurring naturally, contains several predicted ORFs and may influence the phenotype of these mice. In contrast, our Bok  −/−  strain was generated in a pure C57BL/6 genetic background, with no detectable transcript because of targeting of the exon 1 splice donor site along with exon 2 (1).

Is BOK required for apoptosis induced by endoplasmic reticulum stress?